Myricetin modulates streptozotocin–cadmium induced oxidative stress in long term experimental diabetic nephrotoxic rats

• Myricetin is a natural bioflavonoid found in vegetables, fruits and red wines.
• Diabetic rats are more susceptible for cadmium nephrotoxicity.
• Cadmium plays as a cumulative nephrotoxicant whether ingested or inhaled.
• Myricetin can able to reduce cellular ROS content in diabetic nephrotoxic rats.
• Myricetin can able to inhibit lipid peroxidation and enhance cellular antioxidants.

Oxidative stress plays a pivotal role in the development of diabetic nephropathy. The present study was aimed to evaluate the modulatory potential of myricetin on streptozotocin (STZ)–cadmium (Cd) induced oxidative stress in diabetic nephrotoxic rats. Diabetic nephrotoxicity was induced by single intraperitoneal injection of STZ at a dose of (40 mg/kg body weight (b/w)) and Cd as cadmium chloride (CdCl2) (100 p.p.m.). Myricetin was administered to diabetic nephrotoxic rats by intraperitoneally at 1.0 mg/kg b/w for a period of 12 weeks to assess its effects on fasting plasma glucose, plasma insulin, total haemoglobin, glycosylated haemoglobin, lipid peroxidation products viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyl content (PCO) and non-enzymatic antioxidants namely vitamins C and E and reduced glutathione (GSH) and also enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR). Improvement of antioxidant status in myricetin supplemented diabetic nephrotoxic rats revealed its cellular protective effect. Histopathology of liver and kidney confirmed the protective effects of myricetin in diabetic nephrotoxic rats. The outcome of this study concludes that myricetin could be therapeutic flavonol for regulating oxidative mechanism in STZ–Cd induced diabetic nephrotoxic rats.